COPD World News     Week of December 28, 2008

Revolutionary artificial lung set to save thousands of lives

Swansea, Wales - A NEW revolutionary device developed in Wales can “breathe” for people with diseased or damaged lungs. Expected to save thousands of lives across the globe, the artificial lung is also on track to save the NHS millions of pounds.

The portable respiratory aid is the size of a glasses case. And it mimics the function of healthy lungs so it can treat people outside expensive intensive care units, freeing space for others. Designed by hi-tech medical innovations firm Haemair, it can “breathe” for people with a range of life-threatening conditions such as infections or chronic bronchitis and emphysema, which both come under the umbrella term chronic obstructive pulmonary disorder (COPD).

Dr Steve Brown, senior engineer at Haemair, said: “There is urgent need for a device that will support life while patients recover from acute infections. If respiration could be supported without the lungs for just a few weeks, many infections would recover. Thus, people who currently die could go on to lead healthy lives.

”Wales with its long history of mining has one of the highest rates of COPD in the UK. Latest figures show 1,500 people died from the condition in 2006 with thousands more confined to beds or wheelchairs as a result of the debilitating condition. The company, which is based at Swansea University’s Digital Technium, has now won an international award for the device. The Institution of Chemical Engineers (IChemE) Industry Award for Innovation and Excellence 2008 was presented to its researchers, the university announced.

Haemair is now working with Swansea University and Abertawe Bro Morgannwg (ABM) University NHS Trust to bring the device into hospitals. It will begin clinical use next year and is eventually hoped to be a viable alternative to lung transplants. Other applications could include treatment of soldiers exposed to chemical and biological weapons making the military and defence sectors potential customers.

The artificial lung works by taking blood from the body then passing it through a mass exchange device consisting of thousands of hollow fibre membranes. Air is then passed through the tiny tubes and oxygen feeds into the patient’s blood stream while carbon dioxide is taken out of the blood. The blood and air flows are controlled by a complex computer programme.

The 200g device has already notched up two national awards – the 2007 MediWales Award for Partnership with the NHS and the 2007 Technium Award for Most Innovative Company A&E consultant Dr Adrian Evans heads the clinical haemorheology research laboratory at Morriston Hospital, which is using its expertise in handling blood to help develop the device. He said: “This expertise is essential in developing devices that are in contact with blood without causing blood clotting. This is because any device that returns blood clots to the body can lead to complications and endanger the life of a patient.

”Haemair will initially develop external aids that support breathing while patients get better. Ultimately the firm hopes to develop full artificial lungs capable of replacing diseased lungs altogether. Dr Brown said: “The devices are aimed at both acute and chronic lung conditions. This is vital because although people can recover from acute infections, the only treatment for chronic lung failure is a transplant.

“Our treatment is based on a simple principle of not forcing diseased lungs to work harder. We believe this device will not only improve the quality of life for sufferers and avoid long-term lung damage, but will save lives. “What’s more, this should help primary health providers save several thousand pounds per patient by taking patients out of intensive care or high dependency units and into general wards.”

Haemair researchers are also developing a second device. This will place the mass exchanger inside the human body, therefore eliminating the need for a blood pump and pump controller. In the longer term the device offers an alternative to complex lung transplants. Dr Brown said : “Such ‘on demand’ transplant opens up new areas of application, such as early treatment of lung cancer.”

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COPD World News     Week of December 21, 2008

Men With Severe COPD at Increased Risk for Osteoporosis

New York, NY - Men with chronic obstructive pulmonary disease (COPD), including emphysema and chronic bronchitis, may also be at risk for osteoporosis, according to a study published in the December issue of the journal CHEST.

Tadashi Ohara, MD, and Toyohiro Hirai, MD, Department of Respiratory Medicine, Kyoto University, Kyoto, Japan, and colleagues measured vertebral bone density and the percentage of low-attenuation area (LAA%) in the lungs of 65 male patients with COPD using chest computed tomography (CT) scans.
They also investigated the relationships among CT scan measurements, anthropometric parameters, and pulmonary function.

Results showed that LAA% had a significant negative correlation with bone mineral density (BMD), or patients with the most severe COPD had lowest BMD.  In addition, multiple regression analysis showed that only LAA% and body mass index (BMI) were predictive of BMD among age, BMI, smoking index, forced expiratory volume (FEV), arterial blood gas, and LAA%

Although osteoporosis has multiple risk factors, researchers concluded that a systemic effect of COPD may contribute directly to osteoporosis and that chest CT scanning is useful for the management of COPD as a systemic disease.

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COPD World News     Week of December 14, 2008

FDA Advisers Recommend Rejection of Airway Valve for Emphysema

Gaithersburg, Md - An FDA advisory panel recommended today against agency approval of a first-of-its-kind one-way airway valve for emphysema patients, a device billed as a noninvasive substitute for lung volume-reduction surgery.

By an 11-2 vote, the Anesthesiology and Respiratory Therapy Device Panel found insufficient evidence of benefit to outweigh the risks of implanting the Zephyr Endobronchial Valve, manufactured by Emphasys Medical of Redwood City, Cal. The panel was chaired by anesthesiologist David Birnbach, M.D., M.P.H., of the University of Miami. The affirmative votes were from two pulmonologists, Andrew Reis, M.D., of the University of California San Diego, and Philip Marcus, M.D., of the University of Arizona in Tuscan. Drs. Marcus and Reis argued that the panel should recommend approving the device with some caveats, such as demanding an immediate post-market study, but the panel voted against approving the device with added conditions.

"Once you approve, the cat is out of the bag," said panel member Hugh Cassiere, M.D., director of the cardiothoracic unit at North Shore University Hospital in Manhasset, N.Y. "Approving a product just to continue research is not justified," he said. But panel members seemed as upset as the company with the decision. "It kind of breaks my heart to vote against this," said Stephen Li, Ph.D., of the Medical Device Testing and Innovations in Windsor, N.J.

"The panel recognized how few options exist for emphysema patients. The Zephyr device is a removable one-way valve that is implanted by fiberoptic bronchoscopy into the diseased lobe in the lung.

The purported mechanism of the valve is to reduce thoracic gas volume by preventing air from entering while still allowing trapped gas to escape. The device limits the amount of air intake for an emphysema patient, and offers an alternative to the more risky lung volume reduction surgery for some patients, said pulmonologist Frank Sciurba, M.D., of the University of Pittsburgh, who was principal investigator for the key clinical trial, VENT.

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COPD World News     Week of December 7, 2008

Airway Transplant Shows Potential of Stem Cells for Tissue Engineering

Barcelona, Spain - A tissue-engineered airway, using autologous stem cells, has restored lung function and quality of life for a 30-year-old mother of two who suffered from tuberculosis. The transplanted airway -- replacing a collapsed left bronchus -- immediately gave Claudia Lorena Castillo Sánchez a functioning left lung, according to Paolo Macchiarini, M.D., of Hospital Clinic, and colleagues.

Four months after the transplant, the grafted airway had a normal appearance and mechanical properties, as well as functioning vasculature, Dr. Macchiarini and colleagues reported online in The Lancet.  Because of the use of the patient's own stem cells, there has been no sign of rejection and Castillo Sánchez is not on any immunosuppressive drugs."We are terribly excited by these results," Dr. Macchiarini said in a statement.

"Just four days after transplantation, the graft was almost indistinguishable from adjacent normal bronchi," he said. "After one month, a biopsy elicited local bleeding, indicating that the blood vessels had already grown back successfully."As a result of tuberculosis, Castillo Sánchez had chronic tracheitis and end-stage bronchomalacia of the left main bronchus, Dr. Macchiarini and colleagues said.

The trachea was resected and a stent placed in the bronchus, but it was poorly tolerated and was later removed. In March this year, Castillo Sánchez suffered shortness of breath so severe she could no longer look after her children or carry out domestic chores. The classical treatment choice was to remove the lung, but the researchers thought an experimental procedure, which had been successful in animals, might be another option.

"I was scared at the beginning because I was the first patient," Castillo Sánchez said in a statement. But she said the possibility of keeping her lung "represented a unique chance for me to return to a normal life that I am now enjoying with my children and family.

"The procedure began with a 7-cm section of trachea, donated by a woman who had died of brain hemorrhage. The researchers removed connective tissue and cycled the trachea 25 times through a "decellularization" detergent solution.   In the end, the trachea was almost devoid of any remaining cells from the donor, the researchers said.

At the same time, they cultured bronchial epithelial cells from the patient. Also, they removed bone marrow, isolated stem cells, and induced them to differentiate into chondrocytes. In a specially designed bioreactor, the external surface of the donated trachea was seeded with chondrocytes, while the internal surface was seeded with epithelial cells. After 96 hours of culture in the bioreactor, the airway was ready for grafting, the researchers said, with both chondrocytes and epithelial cells adhering almost completely.

A surgical team led by Dr. Macchiarini performed a left posterolateral thoracotomy, resected the left main bronchus, and replaced it with the graft. The patient's left lung "immediately ventilated well," the researchers said. Castillo Sánchez spent two days in intensive care, was moved to a general ward, and discharged 10 days after the procedure.

For more information:

COPD World News     Week of November 30, 2008

New research shows COPD awareness remains low, prevalence high

Ottawa, ON - COPD has a higher hospitalization rate and a higher hospital readmission rate than heart failure, angina, and other serious chronic diseases.

Now, new survey results confirm that COPD affects many more Canadians than previously estimated (1.5 million) and that 69 per cent of Canadians have not heard of COPD. In addition to this, 1.6 million Canadians 40 years or older may currently have undiagnosed COPD based on the Lung Health Test, which means 3 million Canadians may have COPD.  The Lung Association released this data to coincide with World COPD Day and its national awareness campaign.

The numbers we continue to see are staggering. The impact to COPD patients and their families can be devastating," said Nora Sobolov President & CEO of The Lung Association. "More than ever we urgently need a comprehensive and national strategy to address all lung health issues, especially COPD. Now is the time to make this disease a priority."

For people with COPD, flare ups or exacerbations can be brought on by something as simple as a common cold, change in weather, or poor air quality. Often, these flare ups can result in emergency room visits, longer-term hospital stays and, in serious cases, death.

"We have many treatments to manage COPD and reduce hospital admissions; they work best when we catch people early," said Dr. Paul Hernandez, Chair of the Canadian Thoracic Society's COPD Guideline Implementation Committee. "We should be screening the at-risk population more aggressively, so COPD can be caught earlier. We can't emphasize enough the importance of early diagnosis and disease management."

The research demonstrated that COPD awareness among Canadians continues to be low. Sixty-nine per cent of Canadians have not heard of COPD. Compared to other major causes of death in Canada such as cancer or heart attack or stroke, awareness remains far too low. Global studies show COPD affects up to 10 per cent of some populations.

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In the USA new survey suggests growing awareness of COPD

Washington, DC - Awareness of COPD is growing, but few Americans have a thorough understanding of the disease, according to a national survey. The new data show that 64 percent of survey respondents had heard of COPD, compared with 49 percent in a 2004 survey. Among those who reported hearing of COPD, only half recognized the disease as a leading cause of death, and just 44 percent understood it to be treatable.

The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health analyzed results from the annual HealthStyles survey of American public health attitudes, knowledge, practices, and lifestyle habit.

While 74 percent of survey respondents correctly identified shortness of breath as a symptom of COPD, only 5 percent recognized chronic cough as a symptom of the disease. Smoking is attributed to as many as 9 out of ten COPD-related deaths, yet most survey respondents, 66 percent, did not recognize smoking as a risk factor.  This was especially true among the current smokers surveyed. Just 22 percent recognized that their smoking puts them at greater risk for COPD.

NHLBI launched the COPD Learn More Breathe Better campaign in 2007 to increase awareness and understanding of COPD and its risk factors, and to underscore the benefits of early detection and treatment in slowing the disease and improving quality of life. The campaign is supported by more than 20 organizations including leading medical professional societies, patient advocacy groups, and corporate partners in facilitating this public health initiative.

For more information:

COPD World News     Week of November 23, 2008

Why Cigarette Smoke Makes Flu, Other Viral Infections Worse

Boston, MA - A new study by researchers at Yale School of Medicine could explain why the cold and flu virus symptoms that are often mild and transient in non-smokers can seriously sicken smokers. The study also identified the mechanism by which viruses and cigarette smoke interact to increase lung inflammation and damage.

Until recently, scientists haven't been able to explain why smokers have more exaggerated responses to viral infections. Smokers have been more likely than non-smokers to die during previous influenza epidemics and are more prone to chronic obstructive pulmonary disease (COPD). Furthermore, children who are exposed to second-hand smoke have more severe responses when infected with respiratory synctial virus.

The prevailing view has been that cigarette smoke decreases anti-viral responses. But the Yale researchers, lead author Jack A. Elias, M.D., the Waldermar Von Zedtwitz Professor of Medicine and chair of internal medicine at Yale School of Medicine, and first author Min-Jong Kang, M.D., associate research scientist, found the opposite to be true.  Their experiments showed that the immune systems of mice exposed to cigarette smoke from as little as two cigarettes a day for two weeks overreacted when they were also exposed to a mimic of the flu virus. The mice's immune systems cleared the virus normally but the exaggerated inflammation caused increased levels of tissue damage.

"The anti-viral responses in the cigarette smoke exposed mice were not only not defective, but were hyperactive," said Elias. "These findings suggest that smokers do not get in trouble because they can't clear or fight off the virus; they get in trouble because they overreact to it.""It's like smokers are using the equivalent of a sledge hammer, rather than a fly swatter, to get rid of a fly," said Elias.

The team found that mice with viral infections that had been exposed to cigarette smoke had accelerated emphysema and airway scarring. Elias and his team also defined the signaling pathway that mediates this exaggerated innate immune response.

"If the exaggerated responses are verified in human studies, it will be the first explanation for why viral infections are more serious in smokers," said Elias. "Once verified, we can find ways to prevent the destruction of lung tissue and the higher illness and death among smokers."

"These studies have identified molecular pathways that can explain how cigarette smoke exposure and viral infections interact to make breathing problems worse in diseases like COPD," said James P. Kiley, director, Division of Lung Diseases of the National Heart, Lung, and Blood Institute. "With further research, these findings may even lead to more effective drug treatments for COPD."

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If the Gene Fits

Some respiratory professionals out there may not have brushed on their knowledge of DNA and gene sequencing since their undergrad or med school days. If that's the case, you might have to have a quick refresher because of the landmark COPD Gene Study launched earlier this year turns out positively, genetics could play an integral part in respiratory care.

The first of the study's 17 clinical sites began recruiting in March and already have accepted 1,500 patients, well ahead of the projected goals. At this rate, Dr. Crapo said it's possible that they could finish recruitment in just a little more than two years. In addition to perhaps changing the way clinicians view and treat COPD, one of the study's main aims is to provide an extensive national database that the medical community could access to use for analysis or ancillary studies.

If the gene fits, the study may enable clinicians to reduce the large enigma that is COPD into smaller, more manageable subsets that would essentially create a new vocabulary in COPD care.

Study Investigators plan to enroll over 10,000 people to find inherited factors that make some people more likely to develop COPD. It has been proven that cigarette smoking causes COPD; however, only 25% of smokers develop COPD. They want to learn why some smokers get COPD and others do not.

They are looking for current and former cigarette smokers to participate in this study. In order to determine risk factors for developing COPD, they need to study people both with and without COPD.

For a list of Clinical Centers.

COPD World News     Week of November 16, 2008

Asthma Medications May Lend Small Benefit to COPD Patients

Philadelphia, PA - Certain asthma medications may provide marginal improvements in chronic obstructive pulmonary disease patients, according to a meta-analysis.

In an analysis of four placebo-controlled trials of COPD patients, treatment with the leukotriene antagonists zafirlukast (Accolate) and montelukast (Singulair) was associated with significant improvements in both forced expiratory volume in one second (FEV1) and forced vital capacity (FVC).  So reported Minh Nguyen, M.D., and Denise Woo, M.D., of California Pacific Medical Center in San Francisco, at the American College of Chest Physicians meeting here.

"In COPD patients with strong asthmatic or allergic components, I think leukotriene antagonists are a viable option, especially since all the treatments in COPD are really there for symptomatic treatment," Dr. Nguyen said. However, he said, the improvements were small, with a mean increase in FEV1 of 0.0386 L (95% CI 0.0267 to 0.0505) and increase in FVC of 0.1047 L (95% CI 0.062 to 0.1474), meaning that these would not be used as first-line treatment but only after all other options had been exhausted.

"They're not first-line, second-line, even third-line clinically relevant," he said, "but by the time you get to fourth-line and you're really running out of options and if [the patients] have a strong allergic component, I think it's clinically relevant at that point."

Leukotriene anatagonists have proven effects in allergy and asthma, but COPD is believed to be influenced by a different branch of the leukotriene pathway, Dr. Nguyen said. However, some studies have shown reduced levels of leukotriene B4 in patients taking montelukast, and others have demonstrated a correlation between FEV1 and leukotriene C4 levels in COPD patients.

"There shouldn't be any change in FEV1," he said, "but clearly there's some kind of crossover going on." Drs. Nguyen and Woo performed a literature search and identified four randomized placebo-controlled trials examining the use of either montelukast (two) or zafirlukast (two) in patients with confirmed COPD and no history of asthma.Overall, there were 126 patients on active treatment and 127 controls. When the data from the four studies were pooled, patients on active treatment had a mean increase in FEV1 of 0.0987 L (95% CI 0.0097 to 0.1876) and in FVC of 0.0977 L (95% CI 0.034 to 0.1614). The maximum changes occurred between two and three hours after treatment. Using a random-effects model for the meta-analysis, the treatment effects became more modest, but still statistically significant.

The results appear to lend support to the Dutch hypothesis, Dr. Nguyen said, which states that asthma and COPD are variations of each another, with COPD tending toward the progressive end of the spectrum and asthma toward the allergic. Either the thought that COPD and asthma are influenced by different branches of the leukotriene pathway is not applicable, he said, or there is a feedback mechanism whereby inhibiting the leukotrienes in one branch affect levels in the other. Ultimately, though, he said the results of the meta-analysis are hypothesis-generating.

For instance, the results may be used to question how much of the idea that the leukotriene B4 pathway influences COPD and the leukotriene C4 cascade influences asthma is valid. In addition, he said, it remains unclear what the ultimate pathophysiologic and biochemical pathway is that allows the leukotriene antagonists to affect COPD and the leukotriene B4 pathway.

For more information:

COPD World News     Week of November 9, 2008

COPD overdiagnosed by current clinical guidelines

Nijemegen, Holland - Current clinical guidelines to assess airflow obstruction overdiagnose chronic obstructive pulmonary disease (COPD) in middle-aged and elderly patients in primary care, Dutch researchers suggest.

The rate of false-positive diagnoses increases with age when the widely recommended forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) ratio of 0.70 is used, report Tjard Schermer (Radboud University Nijmegen Medical Centre) and colleagues in the European Respiratory Journal.

Clinical guidelines recommend a fixed 0.70 cut-off point for the FEV1/FVC ratio to determine whether or not airflow obstruction is present, regardless of the gender and age of the subject involved.

In this study, the researchers compared the diagnostic outcomes when two definitions for airflow obstruction, both using the FEV1/FVC ratio, were applied to 14,056 patients without COPD referred for a diagnostic spirometry test.

The group used gender- and age-specific "lower limit of normal" cutoff points for FEV1/FVC as a comparison against the current clinical guideline-recommended 0.70. They calculated a sensitivity of 97.9% for the fixed cut-off relative to the lower limit of normal cut-off point for COPD, a specificity of 91.2%, a positive predictive value of 72.0%, and a negative predictive value of 99.5%.

"As spirometry is used as a diagnostic test to verify obstruction (instead of excluding it), these predictive values are insufficient," comment Schermer and colleagues.

The discrepancy between the guideline-recommended FEV1/FVC ratio and the gender- and age-specific lower limit of normal cut-off was more pronounced in older patients, with 33% of those aged 50 years and older misdiagnosed with COPD when the guidelines are used.

Using definitions of airflow obstruction based on lower limits of normal from an appropriate reference population would diminish the rate of false positive interpretations, comment the researchers.

The current burden of COPD on individuals and society is large enough to warrant critical appraisal of the main criterion on which the diagnosis of the disease is based, they add.

For more information:

Smoking Cessation Drug Linked to 1,001 New Serious Adverse Events

Alexandria, VA - The smoking-cessation drug varenicline (Chantix) has been associated with 1,001 serious adverse events, including 50 deaths, during the first quarter of 2008, said a drug-safety watchdog group.

The Institute for Safe Medication Practices said that total put varenicline at the top of its list of drugs associated with serious injuries during the quarter. Heparin was second. The institute's drug-safety watchers include Curt D. Furberg, M.D., Ph.D., of Wake Forest. Since varenicline was approved in 2006, there have been 3,325 reported serious injuries in the U.S., including 112 deaths, the institute said.

Pfizer, which markets varenicline, questioned the institute's conclusions, noting that it analyzed data from the FDA's voluntary adverse event reporting system.  Those reports, the company said, were often unverifiable and lack sufficient medical information to draw any conclusions.

The institute, for its part, said its report may have undercounted the number of adverse events because the FDA's post-market surveillance system is voluntary. The group acknowledged, however, that although "the sum totals of adverse event reports normally provide an accurate overall adverse event profile for a drug, the individual reports themselves do not prove that the drug caused the event described."

The FDA has warned of suicide ideation among patients taking varenicline and the Federal Aviation Administration banned the drug from use by pilots and air traffic controllers. But it wasn't just varenicline that was targeted by the institute.

Overall, the group said there were a "record number of deaths and serious injuries associated with drug therapy" during the first quarter of 2008, with 20,745 injuries and 4,824 deaths. The adverse event rate was 2.4-fold higher than the last quarter of 2007. Medication errors accounted for 7.1% of all serious injuries, the group said.

For more information:

COPD World News     Week of November 2, 2008

Moderate Wine Drinkers Less Likely to Be Hospitalized for COPD

Philadelphia, PA - People who reported consuming one or two alcoholic drinks a day, particularly wine, were about one-quarter less likely to be hospitalized later for chronic obstructive pulmonary disease reported Stanton T. Siu, M.D., of Kaiser Permanente Medical Center in Oakland, Calif.

Most of the apparent benefit appeared to be associated with wine, said Dr. Siu at a poster presentation at the American College of Chest Physicians meeting. The risks of COPD hospitalizations among beer and liquor drinkers, across all levels of drinking relative to abstainers, was close to 1.0. But wine drinkers were significantly less likely to have a COPD hospitalization.

Dr. Siu cautioned that the data do not demonstrate a clear protective effect from moderate drinking. He said other factors that may accompany certain drinking habits -- such as diet, exercise, and other lifestyle factors -- may account for the findings.  On the other hand, some known effects of alcohol might plausibly be beneficial to COPD patients. These include antioxidant, anti-inflammatory, immunostimulant, and bronchodilatory activities.

Dr. Siu and colleagues calculated risks of COPD hospitalization for various levels of drinking, adjusting for age, sex, smoking, education, ethnicity, baseline coronary artery disease symptoms, and known baseline lung disease.  Interestingly, according to Dr. Siu, the risk reduction was the same in people who exclusively drank white wine versus those preferring red.

He said the data hinted at increased COPD hospitalization among ex-drinkers.  This group may be more likely to have underlying diseases that impelled them to stop drinking and that also promote COPD, he suggested.  Dr. Siu added that the same database was analyzed for possible relationships between drinking and asthma treatments. No associations were found, he said.

Limitations to the study included the self-reported data on drinking at a single point and lack of information on factors such as diet and exercise that may have affected participants' risk for COPD.

For more information:

Minimally Invasive Metal Implant Treats Emphysema

Berlin, Germany - A new type of implant for the treatment of severe emphysema, which can be placed using a simple, non-invasive procedure, has made its first appearance at the Annual Congress of the European Respiratory Society (ERS) in Berlin, to considerable acclaim.

This device - though, to date, tested on only a handful of patients - could provide a viable alternative to the invasive treatments currently used, including lung volume reduction surgery and lung transplants. The new, revolutionary approach was presented to the Congress in three scientific communications that provided an assessment of the new device's feasibility and effectiveness.

Nobody at the Congress could fail to be aware that, in Europe alone, over 13.5 million people have chronic obstructive pulmonary disease (COPD). This is an umbrella term, covering both chronic bronchitis and emphysema, conditions which lead to increasingly disabling breathlessness over time and kill 145,000 Europeans each year. COPD's impact on health costs is close to 700 million euros annually.

One of the underlying pathologies, emphysema, is an irreversible condition caused by a loss of elasticity in the lungs following destruction of the walls of the alveoli, small cavities responsible for gas exchange. When these walls are damaged, air becomes blocked in the lung, which begins to swell, making breathing increasingly difficult.

The implant, designed to restore or improve the patient's normal breathing mechanism, is made of super-elastic nitinol (a metal alloy). It aims to compress the lung tissue, restore its elasticity and reduce the excessive swelling of the emphysema-affected lung.

Unlike the current invasive surgical procedures, placement of the implant is carried out using only a bronchoscope, a small, flexible tube inserted in the lungs through the mouth, without any need for surgery or incision.

The end goal is the same as with the standard surgical treatment - to reduce lung volume - but without the need to excise areas of the lung, and without the mortality and morbidity risks that surgery involves. Furthermore, its effectiveness should not be undermined by air bypassing the treated area.

The first triumph, as Herth and his colleagues told the Congress, was that the procedure was found to be safe, and was well tolerated by the patients, aged 61 on average, who were able to go home after three days. The study kept the patients in hospital for 72 hours so that their health could be comprehensively monitored, "but in future patients will be able to go home the next morning", Herth explained.  And, the procedure proved highly effective according to the figures announced in Berlin.

Three-month follow-up showed, for all tests, an observed improvement in lung function, comfort and quality of life for the five patients.  For example, in some patients FEV1 (forced expiratory volume in one second) rose by 18% and patients on average were able to walk an additional 38 metres in the traditional six-minute walking test. Quality of life, measured using the St. George's Respiratory Questionnaire, was found to have improved significantly in four of the five patients.

"This study is highly significant", the Congress was told by Armin Ernst of Beth Israel Deaconess Medical Center, Boston, who represented the American teams. "For the first time, a technology has been designed specifically to restore bronchiolar elasticity. In the future, this will help thousands of patients with emphysema."

On the basis of the results presented in Berlin, other centres throughout Europe will now be able to undertake similar studies.

For more information:

COPD World News     Week of October 26, 2008

New National Guidelines on emergency oxygen uses

London, UK - The first national guideline for the emergency use of oxygen in adults has been published, with the aim of simplifying oxygen delivery and better protecting acutely ill patients. The guideline is published in the October 2008 issue of Thorax, the journal of the British Thoracic Society.

Until now, most healthcare professionals have followed their own institution's customary practice when administering oxygen therapy...Oxygen is one of the most widely used drugs, and is used across the whole range of healthcare specialties.

Oxygen is an extremely important drug because hypoxaemia can cause death during many medical emergencies and it is essential to protect patients from this risk by the rapid recognition of acute illness and hypoxaemia followed by the immediate.

The guideline recommends that oxygen is administered to patients whose oxygen saturation falls below the target saturation ranges (94-98% for most acutely ill patients and 88-92% for those at risk of type 2 respiratory failure with raised carbon dioxide level in the blood), and that those who administer oxygen therapy should monitor the patient and keep within those specified target saturation ranges.

Despite a widespread belief amongst medical staff, and patients, that oxygen relieves breathlessness, there is no evidence that oxygen has an effect on breathlessness if the blood oxygen level is normal. The guideline group advised that too much oxygen can prove harmful in patients with chronic lung diseases such as COPD and 'blind' oxygen therapy outside of critical illness might actually delay recognition of a patient's deterioration by providing a false sense of reassurance based on high oximetry measurements.

More information and an abbreviated copy of the British Thoracic Society's Guideline for Emergency Oxygen Use in Adult Patients for download are available on.

COPD World News     Week of October 19, 2008

Key Component Of Debilitating Lung Disease Identified

Denver, CO - For the first time, researchers have demonstrated a close correlation between the decline in a key component of the lung's antioxidant defense system and the progression of chronic obstructive pulmonary disease (COPD) in humans.

COPD is a degenerative condition that decreases the flow of air through the lungs as the lung's air sacs are damaged. A study of lung tissue samples from COPD patients by scientists at the Johns Hopkins Bloomberg School of Public Health found that expression of the regulating gene NRF2 was significantly decreased in smokers with advanced COPD compared to smokers without COPD.

The study team was led by Shyam Biswal, PhD, an associate professor in the Bloomberg School's Department of Environmental Health Sciences and the Division of Pulmonary and Critical Care Medicine at the Johns Hopkins School of Medicine.

According to Biswal, NRF2 (nuclear factor erythroid-derived 2-related factor 2) works as a "master gene" to turn on numerous antioxidant and pollutant-detoxifying genes to protect the lungs from environmental pollutants, such as cigarette smoke. Biswal previously identified that disruption of NRF2 expression in mice caused early onset and severe emphysema, which is a major component of COPD in human. However, the status of this critical pathway in humans with COPD was unclear.

"This work clearly demonstrates that decline in our antioxidant system is involved in progression of COPD, which could also be the case for other environmental diseases," said Biswal. "There is no treatment of COPD, but NRF2 could be a novel target for the development of new drug therapies."Rubin Tuder, MD, a co-author of the study now with the faculty of the University of Colorado, added, "As we learn how the protective actions of NRF2 are decreased in the course of a lifetime of exposure to cigarette smoke, it opens new venues for the development of novel drugs fitted for individual patients in specific stages of the disease.

"The research was supported by the National Institutes of Health through an investigator- initiated grant, as well as the Specialized Center for Clinically Oriented Research (SCCOR) at the Johns Hopkins School of Medicine. Lung specimens were provided by the Lung Tissue Research Consortium, which is supported by the National Heart, Lung and Blood Institute.

"COPD affects more than 16 million Americans and is the fourth highest cause of death in the United States," said Robert Wise, MD, professor at the Johns Hopkins School of Medicine and director of the Hopkins SCCOR initiative. "It is the only disease among the top 10 causes of death with a rising mortality rate in the United States. It is predicted to be the third largest cause of death by 2020 and has already reached worldwide epidemic proportions."

For more information:

COPD World News     Week of October 12, 2008

Beta-Blockers Benefit COPD Patients Despite Concerns

Rotterdam,The Netherlands - Cardioselective beta-blockers appear to be safe and may improve outcomes for chronic obstructive pulmonary disease (COPD) patients undergoing vascular surgery, researchers found.

Beta-blocker use independently lowered mortality among carefully selected COPD patients by 63% at 30 days and 27% long term, Don Poldermans, M.D., Ph.D., of Erasmus Medical Center here, and colleagues reported in the Oct. 1 issue of the American Journal of Respiratory and Critical Care Medicine.

In their large single-center study, higher doses were particularly effective against short-term mortality, they said. Beta-blockers have often been withheld from COPD patients because of concern over acute bronchospasm and elevated airway hyperresponsiveness from their antagonism of beta-2 receptors, which is linked to mortality, the researchers said.

The reassuring findings add to the evidence that these medications are safe for all patients with COPD who need them for concurrent diseases, said Mario Cazzola, M.D., of the University of Rome "Tor Vergata," and Maria Gabriella Matera, M.D., Ph.D., of the Second University of Naples, in an accompanying editorial. But longer-term data are needed, and "it still seems appropriate to use cardioselective beta-blockers in patients with COPD at the lowest dose and to titrate slowly with attention to lung function and symptoms," they recommended.

Enthusiasm for beta-blockers has recently been dampened for all surgical patients, commented John E. Heffner, M.D., of Providence Portland Medical Center in Portland, Ore., and past president of the American Thoracic Society.

The Perioperative Ischemic Evaluation (POISE) study found higher mortality with the drugs in a general population of patients undergoing non-cardiac surgery, he noted.  "But, COPD is a special subset of patients at particularly high risk of cardiovascular events," Dr. Heffner said. "We will need further studies that will look specifically at COPD patients to determine clearly the risks or benefits of preoperative beta-blocker therapy."

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COPD World News     Week of October 5, 2008

Novel Therapeutic Options Uncovered By Khat Chewing

London, UK - Fresh khat (Catha edulis) leaves have been chewed for centuries in eastern Africa and in the Arabian Peninsula in order to reach a state of euphoria and stimulation. This is due to its main active constituent, cathinone, which increases the release of catecholamines in the brain, evoking an "ampthetamine-like" effect. In these countries, khat has been traditionally used as a social drug.

However, new patterns of khat consumption are now emerging in these countries, and the development of air transportation has contributed to the spread of this habit to the rest of the world. Khat growing, distribution and use are therefore becoming an international issue, as shown by the significant press interest in this substance. Interestingly, fresh khat leaves prepared as an infusion in some African countries are considered a traditional remedy for airway diseases, but until now the precise mechanism of action underlying this effect was unknown.

In this study, Maria Belvisi (National Heart and Lung Institute, Imperial College School of Medicine, London, UK) and her colleagues highlight an inhibitory action of this natural product on cholinergic contractile responses of guinea pig and human airway smooth muscle, and reveal its mechanism of action, thereby uncovering new therapeutic options for the treatment of airway diseases.

This study is the first to address how khat, when used as a traditional remedy, can alleviate respiratory disease symptoms. It shows that cathinone targets both post-ganglionic, pre-junctional a2 adrenergic and 5-HT7 receptors to inhibit the release of acetylcholine from parasympathetic nerves innervating the airways, thereby modulating the neural control of airway constrictor tone.

Indeed, in COPD in particular, increased parasympathetic drive is responsible for increased bronchial smooth muscle tone and excessive mucus production. Muscarinic antagonists (also known as anti- cholinergics, e.g. ipratropium and tiotropium) are particularly effective as bronchodilators in the treatment of COPD where the vagal tone appears to be the only reversible component of airflow limitation. In this respect, the development of new anti-cholinergic molecules based on a mechanism of action other than antagonising muscarinic receptors may be of particular interest in the treatment of airway diseases with heightened cholinergic tone.

Therefore, cathinone, with its original dual pre-junctional mechanism of action, may lead to the development of novel therapeutic approaches for the treatment of such diseases.

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COPD World News     Week of September 28, 2008

Spiriva linked with risk of cardiovascular death and stroke

Chicago, IL - Findings from a meta-analysis published in the current issue of JAMA indicate that Pfizer's and Boehringer Ingelheim's inhaled anticholinergic Spiriva (tiotropium) and ipratropium, marketed by Boehringer Ingelheim as Atrovent, are associated with significantly increased risk of cardiovascular death, myocardial infarction (MI) or stroke among patients with chronic obstructive pulmonary disease (COPD).

The companies released data from a separate analysis of several clinical trials that they say confirm the long-term safety profile of Spiriva.

The JAMA study analysed 17 controlled trials involving 14 783 patients and found that those who took Spiriva or Atrovent for at least one month had a 58-percent greater risk of cardiovascular death, MI or stroke, compared with those who took other treatments or placebo. Specifically, of the patients who took either Spiriva or Atrovent, 1.8 percent experienced cardiovascular death, MI or stroke, whereas 1.2 percent of patients given other drugs or placebo experienced these adverse events.

Lead author Sonal Singh said that the findings suggest "a reassessment of the cardiovascular safety of these agents is needed." Singh added: "This study is questioning whether this drug is safe for COPD patients. Regulatory reaction is needed to explain this risk."

Meanwhile, the drugmakers conducted a separate analysis of 30 placebo-controlled studies involving 19,545 patients with COPD who were randomised to receive either Spiriva or placebo. Results showed that there was no increased risk of death from all causes or death due to cardiovascular events in patients treated with Spiriva.

"We strongly disagree with the conclusion" reached in the study in JAMA, the companies stated. Andreas Barner, Boehringer Ingelheim's vice chairman for R&D, remarked that "our analysis, which includes data from the four-year UPLIFT trial, supports the safety profile of Spiriva."

Commenting on the news, FDA spokesperson Christopher Kelly indicated that "once the complete study report for UPLIFT is submitted, the FDA plans to thoroughly review the data to confirm the preliminary findings for UPLIFT and also review all other available information."

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COPD World News     Week of September 21, 2008

Broccoli Compound Protects Against COPD Damage In Lungs

Baltimore, Maryland - US researchers found that a compound that occurs naturally in broccoli increases the activity of a gene that can protect the lungs against oxidative damage by chronic obstructive pulmonary disease (COPD), a major smoking-related disease. The study could point the way to new therapies that slow the progress of COPD, for which there is currently no effective treatment.

The study is published in the second September issue of the American Journal of Respiratory and Critical Care Medicine and was conducted by researchers from the Johns Hopkins School of Medicine in Baltimore, Maryland.According to the US National Heart, Lung and Blood Institute (NHLBI), COPD, an umbrella term for what used to be called emphysema and chronic bronchitis, is the 4th leading cause of death in the US, where there are 12 million people living with the disease.

There is no effective therapy for COPD, and over time, patients find it increasingly difficult to breathe, as the airways get narrower from inflammation caused by toxins. The World Health Organization (WHO) predicts that by 2030 COPD will be the third major cause of death in the world.

Smoking is the leading cause of COPD. Scientists already knew that a gene called NRF2 regulates a group of antioxidants that appear to go down as the severity of COPD goes up in smokers, and that a substance found in broccoli, an isothiocynate called sulforaphane, increases the activity of this gene. One of the researchers had also shown that disruption in the expression of NRF2 in mice exposed to cigarette smoke triggered early onset of severe COPD.

For this study, the researchers looked at tissue samples from the lungs of smokers with and without COPD to see if there were any differences in NRF2 expression and the proteins that regulate it, such as KEAP1, which inhibits it, and DJ-1, which stabilizes it.Compared to the lungs of smokers without COPD, the lungs of smokers with COPD had much lower levels of NRF2-dependent antioxidants, higher levels of oxidative stress markers and a significant decrease in NRF2 protein. There was however no change in NRF2 mRNA levels (showing that the gene was switched on and expressing the protein, but this was later being degraded). Also, levels of KEAP1 were the same for both groups, but the tissue from the smokers showed a significant drop in DJ-1.

In an accompanying editorial, Dr Peter Barnes, of the National Heart and Lung Institute in London, wrote: "Increasing NRF2 may also restore important detoxifying enzymes to counteract other effects of tobacco smoke.""This has been achieved in vitro and in vivo by isothiocynate compounds, such as sulforaphane, which occurs naturally in broccoli and [wasabi]."Isothicyanates, like the ones found in broccoli, inhibit KEAP1 and thus stop it degrading NRF2, wrote Barnes, and sulforapane has been shown to restore antioxidant gene expression in human epithelial tissue where DJ-1 has been reduced.

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COPD World News     Week of September 14, 2008

Smoking riskier to women's hearts than men's

MUNICH, Germany - Women typically get heart disease much later than men, but not if they smoke, researchers here have determined. In fact, women who smoke have heart attacks more than a dozen years earlier than women who don't smoke, Norwegian doctors reported in a study presented to the European Society of Cardiology. For men, the gap is not so dramatic; male smokers have heart attacks about six years earlier than men who don't smoke.

"This is not a minor difference," said Dr. Silvia Priori, a cardiologist at the Scientific Institute in Pavia, Italy. "Women need to realize they are losing much more than men when they smoke," she said. Priori was not connected to the research. Dr. Morten Grundtvig and colleagues from the Innlandet Hospital Trust in Lillehammer, Norway, based their study on data from 1,784 patients admitted for a first heart attack at a hospital in Lillehammer.

Their study found that the men on average had their first heart attack at age 72 if they didn't smoke, and at 64 if they did. Women in the study had their first heart attack at age 81 if they didn't smoke, and at age 66 if they did.

That works out to eight and 15 years, respectively, for men and women. After adjusting for other heart risk factors like blood pressure, cholesterol and diabetes, researchers found that the difference for men was about six years for women about 14 years. Previous studies looking at a possible gender difference have been inconclusive.

Doctors have long suspected that female hormones protect women against heart disease. Estrogen is thought to raise the levels of good cholesterol as well as enabling blood vessel walls to relax more easily, thus lowering the chances of a blockage.

Grundtvig said that smoking might make women go through menopause earlier, leaving them less protected against a heart attack. With rising rates of smoking in women - compared with falling rates in men - Grundtvig said that doctors expect to see increased heart disease in women.

"Smoking might erase the natural advantage that women have," said Dr. Robert Harrington, a professor of medicine at Duke University and spokesman for the American College of Cardiology. Doctors aren't yet sure if other cardiac risk factors like cholesterol and obesity also affect women differently. "The difference in how smoking affects women and men is profound," Harrington said. "Unless women don't smoke or quit, they risk ending up with the same terrible diseases as men, only at a much earlier age."

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COPD World News     Week of September 7, 2008

Common infection may increase risk for COPD

Denver, CO - Mycoplasma pneumoniae (Mp), an infection that often goes undetected, can block the natural protective response of the lung against tobacco smoke, according to US researchers. The findings could point to a mechanism that may cause smokers to develop chronic obstructive pulmonary disease (COPD), Brian Day and colleagues from the National Jewish Medical & Research Center in Denver, Colorado, explain in the Journal Infection and Immunity.

"Although smoking is the overwhelming cause of chronic obstructive pulmonary disease (COPD), only 20% of smokers develop the disease," Day said. "Our findings suggest that Mp infection may be one of the co-factors that lead to COPD and other diseases among smokers."

Chronic cigarette smoking evokes a lung glutathione adaptive response that results in elevated glutathione levels, but previous studies have indicated that lung infections might affect the protective response of the lung. Mp is a common lung pathogen and the most common cause of pneumonia, but can be difficult to detect because it is challenging to grow in culture. Day and team infected mice with Mp, and found it had a mild effect, slightly lowering glutathione levels in the lungs of mice breathing fresh air. However, mice that were exposed to tobacco smoke and then infected with Mp had significantly reduced glutathione levels.

"The Mp infection completely blocked the protective response mice normally mount against tobacco smoke, reducing antioxidant levels well below even those of mice breathing fresh air," said Day.

In addition, the team found that mice exposed to tobacco smoke and Mp had much higher levels of oxidized glutathione and lower levels of reduced glutathione, along with significantly lowered levels of the enzyme glutathione reductase.

"The Mp infection blocked the lungs' protective response to tobacco smoke by lowering levels of the enzyme that normally recycles oxidized glutathione back into its protective, reduced form. This resulted in severe oxidative stress and increased tissue damage as measured by oxidized DNA.  These higher levels of oxidative stress and damage are likely to predispose smokers with Mycoplasma infections to lung disease, such as COPD or cancer. These studies suggest Mp infection synergizes with ETS and suppresses the lung's ability to respond appropriately to environmental challenges leading to enhanced oxidative stress," said Day.

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COPD World News     Week of August 31, 2008

Unrecognized myocardical infarctions common in patients with COPD

Lorenskog, Norway - Many patients receiving hospital treatment for chronic obstructive pulmonary disease (COPD) show evidence of having previously suffered a myocardical infarction, but less than a third of such patients have received a previous myocardical infarction diagnosis, study results suggest.

The findings also indicate that many COPD patients who have suffered myocardical infarctions are missing out on effective treatment to minimize heart damage.  P. Brekke and colleagues from Akershus University Hospital in Lorenskog, Norway, explain: "Patients with COPD are usually former or current smokers, and are at increased risk of... heart disease."

To assess the prevalence of myocardical infarction among COPD patients, the authors assessed hospital data on 827 patients who had received hospital treatment for a COPD exacerbation between 2000 and 2003. All the patients underwent an electrocardiogram at hospital admission.

A total of 229 patients had electrocardiogram results indicative of having previously suffered a myocardical infarction. However, examination of these patients' medical records revealed that just 30% had received a myocardical infarction diagnosis. Furthermore, female patients with COPD who had evidence of previous heart attack were less likely to have received a diagnosis than their male counterparts.

The researchers conclude in the Journal Respiratory Medicine: "Our study suggests that myocardial infarction is frequently unrecognised in patients hospitalized for COPD."

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COPD World News     Week of August 24, 2008

Study reports that Advair slows progression of COPD

Boston, MA - For the first time, studies have shown that pharmacotherapy can slow the progression of chronic obstructive pulmonary disease, researchers here said. In a large randomized controlled trial, the combination of fluticasone proprionate and salmeterol (Advair) reduced the decline in one-second forced expiratory volume FEV1 by 16 mL a year compared with placebo, according to Bartolomi Celli, M.D., of Tufts, and colleagues.  

The study data published in the American Journal of Respiratory and Critical Care Medicine showed that GlaxoSmithKline's Advair (salmeterol/fluticasone) slows the progression of chronic obstructive pulmonary disease compared with placebo.

In a post-hoc analysis of the TORCH study, which involved more than 6000 patients with the disease, the findings demonstrated that Advair decreased the rate of lung function decline by more than 50 percent, compared with placebo. The results also showed that patients who received either salmeterol or fluticasone alone had a lower rate of lung function decline, compared with those who received placebo.

Bartolomi Celli, the lead author of the study, commented that "the main finding is that for the first time, it's been shown that administering pharmacotherapy to patients with COPD can change and modify the clinical course of their disease."

Dr. Celli and colleagues concluded that pharmacotherapy with the two drugs can slow the progression of COPD -- the only intervention other than smoking cessation that has been shown to do so.

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COPD World News     Week of August 17, 2008

Untreated Sleep-Disordered Breathing May Triple Risk for Mortality

Madison, WI - An 18-year follow-up study finds that untreated sleep-disordered breathing (SDB) increases the risk for mortality 3-fold, according to the results of a study reported in the August 1 issue of Sleep.

"...SDB is a treatable but markedly under-diagnosed condition of frequent breathing pauses during sleep," write Terry Young, PhD, from the University of Wisconsin-Madison, and colleagues. "SDB is linked to incident cardiovascular disease, stroke, and other morbidity. However, the risk of mortality with untreated SDB, determined by polysomnography screening, in the general population has not been established."

The study cohort for this 18-year mortality follow-up study was the population-based Wisconsin Sleep Cohort sample (n = 1522). Participants had baseline polysomnography to detect SDB, which was characterized by the number of apnea and hypopnea episodes per hour of sleep. Cutoff points at 5, 15, and 30 episodes per hour of sleep identified mild, moderate, and severe SDB, respectively. All-cause and cardiovascular mortality risks associated with SDB severity levels, after adjustment for potential confounding factors, were estimated with use of Cox proportional hazards regression.

"Our findings of a significant, high mortality risk with untreated SDB, independent of age, sex, and BMI [body mass index] underscore the need for heightened clinical recognition and treatment of SDB, indicated by frequent episodes of apnea and hypopnea, irrespective of symptoms of sleepiness," the study authors write.

Limitations of this study include lack of information on consistent CPAP use with time or effectiveness of air pressure level to prevent airway closure, lack of randomization, inability to determine how CPAP contributes to lower death rates, inability to determine how long participants had SDB before their baseline study, and cohort 95% white and all employed at recruitment.

"Although further studies are needed to quantify the proportion of mortality that could be lowered by prevention or treatment of SDB, the results of our study can be applied directly to current health care practice," the study authors conclude.

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COPD World News     Week of August 10, 2008

Uninsured Americans Carry Large Chronic Disease Burden

CAMBRIDGE, Mass.- Nearly one-third of uninsured Americans under age 65 reported having cardiovascular disease, diabetes, hypertension, or some other chronic condition, researchers here said.

Data from the National Health and Nutrition Examination Survey (NHANES) showed that percentages of uninsured people reporting a chronic condition ranged from 11.9% for hypercholesterolemia, to 19.3% for asthma and COPD, 19.6% for cardiovascular disease, 15.5% for hypertension, 16.6% for diabetes mellitus and 15.4% for a previous cancer - reported Andrew P. Wilper, M.D., M.P.H., of Cambridge Health Alliance, and colleagues in the Aug. 5 issue of Annals of Internal Medicine.

Some 31.3% of the uninsured had at least one of the six conditions, the researchers said.  "These findings counter notions that persons without insurance are a largely healthy population with little need for ongoing medical care," Dr. Wilper and colleagues wrote.  The researchers said 45.4% of insured patients had at least one chronic disease. The higher percentage was likely because they were older on average than the uninsured, they said.

In June, the CDC reported that about 43 million Americans, 14.5% of the overall population, were uninsured in 2007. Dr. Wilper and colleagues found that, after adjusting for age, sex, and race/ethnicity, lack of insurance significantly predicted a lower likelihood of seeing a health professional in the past year.  Those without insurance were also more likely to name an emergency department as their standard site of care and to report not having a standard site of care.

"For some of the 11.4 million uninsured Americans with serious chronic conditions, access to care seems to be unobtainable; many may face early disability and death as a result," Dr. Wilper and colleagues wrote. They pointed out that treatments for the six chronic conditions are both standard and a national priority. The researchers suggested that a healthcare system with a de facto exclusion based on insurance status is unethical.

In an accompanying editorial, Marshall H. Chin, M.D., M.P.H., of the University of Chicago, commented that ensuring good treatment for chronic disease will require more than health insurance reform."It will not be sufficient unless it is coupled with quality improvement efforts targeting the reasons that vulnerable populations with access to care often do not receive optimal care," he wrote.

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COPD World News     Week of August 3, 2008

Group therapy helps hospitalized COPD patients quit smoking

Glostrup, Denmark - Patients with chronic obstructive pulmonary disease (COPD) are more likely to quit smoking if they are offered smoking cessation programs rather than standard anti-smoking information at the same time as receiving hospital treatment, Danish researchers report.

Getting patients to quit is the most important factor in the treatment and rehabilitation of patients, Anders Borglykke (Glostrup University Hospital) and colleagues explain in the Clinical Respiratory Journal. However, the authors note, until now there has been little investigation into the effect of smoking cessation programs in patients hospitalized by COPD.

Borglykke and team studied 121 patients with COPD who were offered a smoking cessation program while receiving hospital treatment for an exacerbation of their disease, and 102 COPD patients who were not offered smoking cessation help while in hospital. All of the patients received standard information on the benefits of quitting smoking.

A total of 48 patients chose to participate in the smoking cessation program, which included weekly 2-hour group sessions with professional cessation advice, supported by nicotine replacement therapy. The patients' spouses were also encouraged to participate in these group sessions in a supportive role.

After 1 year, the team found that 36 of the patients who took part in the smoking cessation program had quit smoking compared with just 13 patients offered standard information only. In addition, patients who quit smoking reported significantly less phlegm, and had slightly better survival rates after 1 year than the other patients. After 3 years, the intervention group had significantly fewer total days admitted to hospital and days hospitalized with COPD than patients who received standard information only.

This study shows that an intervention consisting of offering participation in an smoking cessation group to chronic patients makes it possible to obtain higher abstinence rates," Borglykke and team write. They conclude: "As this study is done in a real-life setting, the results are promising and stress the need for further action in order to implement smoking cessation intervention to all patients hospitalised with symptoms of exacerbation of chronic obstructive pulmonary disease.

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COPD World News     Week of July 27, 2008

Secondhand Smoke Increases Spousal Stroke Risk

BOSTON, MA - Secondhand smoke in the home appears to increase the risk of stroke for a non-smoking spouse, researchers here said.

The finding emerged from a prospective analysis of 16,225 married volunteers in the Health and Retirement Study, who were stroke-free when the study began, according to Maria Glymour, Sc.D., of the Harvard School of Public Health, and colleagues.

Over an average of 9.1 years of follow-up, there were 1,130 strokes among the volunteers, who were 50 or older at baseline, Dr. Glymour and colleagues said in the September issue of the American Journal of Preventive Medicine.

The participants were stratified according to sex and their own smoking status -- never-smokers, former smokers, and current smokers, the researchers said. Smoking status referred to cigarettes and did not include pipe or cigar use.

Cox proportional hazards analyses were adjusted for a range of factors including age, race, Hispanic ethnicity, obesity and overweight, alcohol use, and medical conditions such as diagnosed hypertension, diabetes, or heart disease.

The analysis found: Among never-smokers, having a spouse who was a current smoker predicted a 42% increase in stroke hazard, compared with non-smoking couples. The hazard ratio was 1.42, with a 95% confidence interval from 1.02 to 1.92.

Among former smokers, current spousal smoking was associated with a 72% increase in risk, compared with former smokers whose spouses had never smoked. The hazard ratio was 1.72, with a 95% confidence interval from 1.31 to 2.24. Among current smokers, having a spouse who smoked did not increase stroke risk. Compared with couples in which neither partner had ever smoked, the risk for both spouses was elevated if either partner was a current smoker.

So former smokers married to current smokers had a hazard ratio for stroke of 1.80, with a 95% confidence interval from 1.40 to 2.37, the researchers said, and current smokers married to current smokers had a hazard ratio for stroke of 1.87, with a 95% confidence interval from 1.50 to 2.48. There was no evidence that former spousal smoking increased stroke risk or that spousal smoking increased risk among current smokers, Dr. Glymour and colleagues said.

The findings are consistent with a growing body of evidence, the researchers said, although they differ from recent National Health and Nutrition Examination Survey (NHANES) results that suggested a husband's smoking status increased the risk of stroke only among smoking women.

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COPD World News     Week of July 20, 2008

Study Suggests Genetic Factors in Smoking may Increase Risk of Chronic Bronchitis

Stockholm, Sweden - While smoking is the leading risk factor for chronic bronchitis, genes also play a major role in the development of the disease, a recent Swedish study reports.

A recent study, published in the first issue for March of the American Journal of Respiratory and Critical Care Medicine, highlights the importance of genes in the development of smoking-related respiratory diseases, such as chronic bronchitis.

The study, which analyzed data on more than 40,000 Swedish twins born in 1958 or earlier, found that inherited genes accounted for 40% of the risk for chronic bronchitis and that 14% of the genetic risk was also linked to a genetic predisposition to smoke, whether or not a person actually smoked.

The study, which analyzed data on more than 40,000 Swedish twins born in 1958 or earlier, found that inherited genes accounted for 40% of the risk for chronic bronchitis and that 14% of the genetic risk was also linked to a genetic predisposition to smoke, whether or not a person actually smoked.

The researchers analyzed data from the Screening Across Lifespan Twin (SALT) study in Sweden, which surveyed all known living twins in Sweden born in 1958 or earlier. The investigators used the survey data and statistical modeling to determine the extent to which the genetic and environmental influences that comprise an individual's risk of developing chronic bronchitis were responsible for disease progression.

Jenny Hallberg of the Department of Public Health Sciences at the Karolinska Institutet, Stockholm, cautioned that the finding that the genetic factors contributing to chronic bronchitis were largely independent of those that contribute to smoking should not be interpreted to mean that smoking has no effect on chronic bronchitis. "Although there was some genetic interplay, it is safe to say that smoking itself, and not the genes that predispose one to smoking, is a larger risk factor in developing chronic bronchitis of environmental exposures primarily smoking than genetic predisposition. This is true in both men and women," said Hallberg.

The research team is currently working on a clinical follow-up study that relates clinical measures of lung function to obstruction. "We believe that it is important to also include testing of lung function to disentangle whether there are genetic differences by sex," stated Hallberg. "There is also data in the literature that social factors have different importance for smoking behavior in men and women. We know much less regarding the genetic influences."

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COPD World News     Week of July 13, 2008

United Kingdom smokers quit in record numbers

London, UK - It's been one year since the UK instituted a broad-based smoking ban and it is now predicted that the rapid decrease in smoking could save 40,000 lives in the next ten years.

A year ago, if you'd asked Professor Robert West to predict the effect that the smoking ban in England would have on smokers he would have reckoned on no change. Yet tomorrow, on the first anniversary of the legislation that banned smoking in public places, he will announce that an estimated 400,000 people have given up since it came into force. This represents a dramatic increase in the rate at which regular smokers are quitting.

Smoking rates have gone down by five percentage points over nine months, an average increase of 0.6 per cent each month, compared with 0.2 per cent before the ban. This means that three times as many smokers are now quitting than in the nine months before the ban. "This is not as I expected and it's dramatic," says West, Cancer Research UK's director of tobacco studies. "Up to April this year, [smoking] prevalence is 4 per cent lower than it would otherwise have been, which we've never seen in this country before."

West's figures are based on a monthly study of 1,700 smokers throughout England where an estimated 9.5 million people smoke, accounting for 20 per cent of the adult population. "Even at this rate we're talking about 70,000 deaths a year," says West. Already it is clear that, by reducing passive smoking, the ban is saving lives. There were 1,384 fewer heart attacks in England in the nine months after the ban.

"The reason is that passive smoke is like bad pollution" West explains. "When people who've got dodgy cardiovascular systems inhale particulate matter at that concentration it can trigger a heart attack immediately. I would estimate that if we stick with what we've achieved, we will save around 40,000 lives over the next ten years from cancer, heart disease and chronic constructive pulmonary disease."

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COPD World News     Week of July 6, 2008

Panic-stricken COPD patients more sensitive to increased inspiratory loads

Sydney, Australia -  Patients with chronic obstructive pulmonary disease (COPD) who also suffer from panic attacks are more sensitive to increased inspiratory loads, Australian researchers report.

The result reinforces the influence of psychologic factors on symptom perception in [COPD]," David McKenzie (Prince of Wales Hospital, Sydney) and colleagues explain in the latest issue of the American Journal of Respiratory and Critical Care Medicine.

Panic attacks are 10 times more common in patients with COPD than in the general population, the authors explain. However, it is not clear how panic attacks influence respiratory symptoms.

McKenzie and team measured perceived dyspnea in response to increasing inspiratory resistive loads (modified Borg Scale) in 20 COPD patients who suffered from panic attacks and 20 who did not, along with 20 healthy controls. Dyspnea ratings increased for all groups as resistive loads increased, but patients with panic attacks or panic disorder rated their level of dyspnea significantly higher than COPD patients without panic attacks and healthy controls.

On average, controls rated their breathing difficulty in response to the highest load as 3.0 (moderate), COPD patients without panic attacks rated it as 4.0 (considerable), whereas COPD patients with panic attacks rated it as 5.6 (severe).  "Increased anxiety led to heightened, not blunted, sensitivity to the inspiratory loads," the authors write.

This finding could have important implications for the management of COPD-related anxiety, McKenzie and team explain, as panic disorder in COPD can be improved by cognitive behavioral therapy even in the absence of any improvement in pulmonary function.

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